Intronic microRNA suppresses endothelial nitric oxide synthase expression and endothelial cell proliferation via inhibition of STAT3 signaling

2011 ◽  
Vol 357 (1-2) ◽  
pp. 9-19 ◽  
Author(s):  
Limei Yan ◽  
Hong Hao ◽  
Terry S. Elton ◽  
Zhenguo Liu ◽  
Hesheng Ou
Keyword(s):  
Nitric Oxide ◽  
Cell Proliferation ◽  
Endothelial Cell ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Endothelial Cell Proliferation ◽  
Stat3 Signaling ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

The smoking-associated oxidant hypothiocyanous acid induces endothelial nitric oxide synthase dysfunction

2013 ◽  
Vol 457 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Jihan Talib ◽  
Jair Kwan ◽  
Aldwin Suryo Rahmanto ◽  
Paul K. Witting ◽  
Michael J. Davies
Keyword(s):  
Nitric Oxide ◽  
Enzyme Activity ◽  
Endothelial Cell ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Monomer Form

The smoking-associated oxidant hypothiocyanous acid converts active dimeric endothelial cell nitric oxide synthase into its monomer form, decreases enzyme activity and releases Zn2+. This is ascribed to targeting of the critical Zn2+–thiol cluster by this thiol-specific oxidant.

scholarly journals Role of Endothelial Nitric Oxide Synthase in Endothelial Cell Migration

1999 ◽  
Vol 19 (5) ◽  
pp. 1156-1161 ◽  
Author(s):  
Toyoaki Murohara ◽  
Bernhard Witzenbichler ◽  
Ioakim Spyridopoulos ◽  
Takayuki Asahara ◽  
Bo Ding ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Migration ◽  
Endothelial Cell ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Endothelial Cell Migration ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Are voltage-dependent ion channels involved in the endothelial cell control of vasomotor tone?

2007 ◽  
Vol 293 (3) ◽  
pp. H1371-H1383 ◽  
Author(s):  
Xavier F. Figueroa ◽  
Chien-Chang Chen ◽  
Kevin P. Campbell ◽  
David N. Damon ◽  
Kathleen H. Day ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Electrical Stimulation ◽  
Endothelial Cell ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Long Distance ◽  
Voltage Dependent ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Vessel Axis

In the microcirculation, longitudinal conduction of vasomotor responses provides an essential means of coordinating flow distribution among vessels in a complex network. Spread of current along the vessel axis can display a regenerative component, which leads to propagation of vasomotor signals over many millimeters; the ionic basis for the regenerative response is unknown. We examined the responses to 10 s of focal electrical stimulation (30 Hz, 2 ms, 30 V) of mouse cremaster arterioles to test the hypothesis that voltage-dependent Na+ (Nav) and Ca2+ channels might be activated in long-distance signaling in microvessels. Electrical stimulation evoked a vasoconstriction at the site of stimulation and a spreading, nondecremental conducted dilation. Endothelial damage (air bubble) blocked conduction of the vasodilation, indicating an involvement of the endothelium. The Nav channel blocker bupivacaine also blocked conduction, and TTX attenuated it. The Nav channel activator veratridine induced an endothelium-dependent dilation. The Nav channel isoforms Nav1.2, Nav1.6, and Nav1.9 were detected in the endothelial cells of cremaster arterioles by immunocytochemistry. These findings are consistent with the involvement of Nav channels in the conducted response. BAPTA buffering of endothelial cell Ca2+ delayed and reduced the conducted dilation, which was almost eliminated by Ni2+, amiloride, or deletion of α1H T-type Ca2+ (Cav3.2) channels. Blockade of endothelial nitric oxide synthase or Ca2+-activated K+ channels also inhibited the conducted vasodilation. Our findings indicate that an electrically induced signal can propagate along the vessel axis via the endothelium and can induce sequential activation of Nav and Cav3.2 channels. The resultant Ca2+ influx activates endothelial nitric oxide synthase and Ca2+-activated K+ channels, triggering vasodilation.

scholarly journals Propofol Depresses Angiotensin II–induced Cell Proliferation in Rat Cardiac Fibroblasts

2010 ◽  
Vol 112 (1) ◽  
pp. 108-118 ◽  
Author(s):  
Tzu-Hurng Cheng ◽  
Yuk-Man Leung ◽  
Chi-Wai Cheung ◽  
Cheng-Hsien Chen ◽  
Yen-Ling Chen ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Proliferation ◽  
Protein Kinase ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Protein Kinase B ◽  
Cardiac Fibroblasts ◽  
Ang Ii ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Background Propofol may have beneficial effects on the prevention of angiotensin II (Ang II)-induced cardiac fibroblast proliferation via its antioxidative properties. The authors hypothesized that propofol may alter Ang II-induced cell proliferation and aimed to identify the putative underlying signaling pathways in rat cardiac fibroblasts. Methods Cultured rat cardiac fibroblasts were pretreated with propofol then stimulated with Ang II; cell proliferation and endothelin-1 gene expression were examined. The effect of propofol on Ang II-induced nicotinamide adenine dinucleotide phosphate-oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, and activator protein 1-mediated reporter activity were also examined. The effect of propofol on nitric oxide production and protein kinase B and endothelial nitric oxide synthase phosphorylations were also tested to elucidate the intracellular mechanism of propofol in proliferation. Results Ang II (100 nm) increased cell proliferation and endothelin-1 expression, which were partially inhibited by propofol (10 or 30 microm). Propofol also inhibited Ang II-increased nicotinamide adenine dinucleotide phosphate-oxidase activity, reactive oxygen species formation, extracellular signal-regulated kinase phosphorylation, and activator protein 1-mediated reporter activity. Propofol was also found to increase nitric oxide generation and protein kinase B and nitric oxide synthase phosphorylations. Nitric oxide synthase inhibitor (N-nitro-L-arginine methylester) and the short interfering RNA transfection for protein kinase B or endothelial nitric oxide synthase markedly attenuated the inhibitory effect of propofol on Ang II-induced cell proliferation. Conclusions The authors' results suggest that propofol prevents cardiac fibroblast proliferation by interfering with the generation of reactive oxygen species and involves the activation of the protein kinase B-endothelial nitric oxide synthase-nitric oxide pathway.

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